"We find that recombinant leptin, either alone or combined
with low-dose insulin therapy, provides equivalent or superior
glycemic stability without the increase in body fat and
up-regulation of cholesterologenic and lipogenic transcription
factors and enzymes observed with insulin monotherapy,"
the
study stated.
"These findings raise the possibility of a role
for leptin supplementation in the treatment of human
T1DM."

One of the researchers, Dr.
Roger
Unger
at the University of Texas Southwestern Medical School,
told the North County Times he's applied to federal regulators to
conduct human clinical trials of the therapy to see if it works in
people. Those interested in more information should email Katherine
Morales at katherine.morales@utsouthwestern.edu.

The study could be highly significant for
Amylin Pharmaceuticals
, which supplied the
recombinant leptin used in the mice. If the results can be
duplicated in humans, it would expand the uses Amylin may pursue to
commercialize its drug.

While insulin has transformed Type I diabetes from a fatal to a
manageable one, the study said, insulin therapy fails to return the
patient to a metabolically normal state. That's because there's a
"disparity" between the insulin needs of
alpha cells
and liver cells, which require higher doses of
insulin, compared to fat cells and muscle, which require lower
doses.

"Peripherally injected insulin can meet all of these
disparate needs only with insulin doses that far exceed the needs
of peripheral sites, causing hypoglycemia,"
the study
said.

But leptin increases insulin's effectiveness, the study said, so
it's active at appropriate levels in various parts of the body.

Leptin caused a big fanfare when its function was announced in
1995, as a potentially blockbuster weight-loss drug. It caused
obese mice to slim down dramatically. However, the effect didn't
last in obese humans, who appear to be leptin-resistant.

But there has been a renaissance of interest in leptin in recent
years: